ABSTRACT Support is requested for a Keystone Symposia conference entitled Cell Death and Inflammation, organized by Drs. Seamus J. Martin and John Silke. The conference will be held in Dublin, Ireland from May 29 - June 2, 2017. Cell death has long been known to be an important instigator of inflammation in sterile injury, as well as an amplifying factor in infection-associated inflammation, but the specific molecules underpinning this remain obscure. Many well-known physiological drivers of cell death (e.g., TNF, TRAIL, CD95/Fas), as well as the molecules that transduce signals from these receptors (e.g., RIPKs, IAPs, TRAFs, IKKs), are also centrally involved in promoting inflammation. However, the tremendous overlap between cell death and inflammatory signaling has only recently been appreciated, and although it is also widely accepted that the constituents of healthy cells can drive inflammation upon release into the extracellular space, the identity of these cellular constituents is still a matter of debate. Therefore, understanding how dead and dying cells initiate and escalate inflammation has important implications for our understanding and treatment of auto-inflammatory and infectious diseases. This conference will explore current knowledge concerning the cellular constituents that drive inflammation (i.e., damage-associated molecular patterns), as well as how abnormal modes of cell death, such as necrosis, necroptosis and NETosis, can perturb inflammatory outputs and responses to dying cells. Participants will focus on teasing out the relationships between cell death and inflammatory signaling to highlight how perturbation of either of these processes invariably impacts upon the other. The molecules that promote and modulate inflammation during cell death will be addressed and gaps in our current understanding of how dead and dying cells influence inflammatory responses in disease settings will be explored. Importantly, the conference will bring together experts in two major research fields that would not normally interact, ?cell death? and ?inflammation,? for the purpose of clarifying what the key questions and therapeutic targets are in this rapidly evolving area.